Quick! If your doctor or dietitian still says you should eat a low-fat diet for your heart’s sake, find another one. In the final of a two-part series, Scottish GP Dr Malcolm Kendrick explains why so many doctors and dietitians dish up junk about cholesterol.

And why everything the experts have been telling you about saturated fat, its impact on LDL, and its impact on CVD is – frankly – ‘complete bollocks’. – Marika Sboros

By Malcolm Kendrick

Just to re-cap. Saturated fat (any fat) is absorbed from the gut and packed into chylomicrons. These travel around the body, losing fat, and shrink down to a chylomicron remnant – which is then absorbed by the liver. There is no connection between chylomicrons and LDL.

Dr Malcolm Kendrick

Instead, LDL comes from VLDL. VLDLs are made in the liver, they contain fat and cholesterol. VLDLs leave the liver, travel around the body and lose fat, shrinking down to become an LDL.

As the only source of LDL is VLDL, this leads to the next obvious question. What makes VLDL levels rise? Well, it sure as hell isn’t fat in the diet. What causes VLDL levels to rise is eating carbohydrates. The next quote is a bit jargon heavy but worth including.

‘De novo lipogenesis is the biological process by which the precursors of acetyl-CoA are synthesized into fatty acids [fats]. In human subjects consuming diets higher in fat (> 30 % energy), lipogenesis is down regulated and extremely low; typically < 10 % of the fatty acids secreted by the liver. This percentage will increase when dietary fat is reduced and replaced by carbohydrate.’

To simplify this as much as possible. If you eat more carbohydrates than your body needs or can store, the liver converts the excess (primarily fructose and glucose) into fat in the liver. This process is called de novo lipogenesis (DNL) The fats that are synthesized are saturated fats and only saturated fats. Once synthesized they are then packed into VLDLs and sent out of the liver.

In short, if you eat fat, the VLDL level falls. If you eat carbohydrates the VLDL level rises. Which is pretty much what you would expect to see.

Moving the discussion on, as VLDLs are the only source of LDL. you now have a conundrum to solve. How can you connect saturated fat intake to a rise in LDL levels, when saturated fat consumption reduces VLDL synthesis? What is the mechanism? The mechanism does not exist!

You could counter by saying, what of the many studies that have shown a fall in LDL when saturated fats are replaced by polyunsaturated fats? Well, this seems to have been shown often enough for me to believe it may even be true.

The explanation for this finding is most likely the fact that, in these studies, saturated fats were replaced by polyunsaturated fats, from plant oils. Plant oils contain stanols (the plant equivalent of cholesterol).

Stanols are known to lower LDL levels, see under Benecol and other suchlike ‘low fat’ spreads. Because stanols compete with cholesterol for absorption there is an impact on the ‘measured’ LDL levels. What this means, in turn, is that the studies that demonstrate a lower LDL, with a reduction in saturated fat consumption, fall foul of the two variables problem.

Namely, if you change two variables in an experiment at the same time, you cannot say which of the variables was responsible for the effect you have seen. Was it the reduction in saturated fats, or the increase in plant stanols, that lowers LDL?

‘In a meta-analysis of over 60 trials, higher intakes of saturated fat were associated with increases in both LDL-C and high-density lipoprotein cholesterol (HDL-C) and decreases in triglyceride levels [VLDL}, for a net neutral effect on the ratio of total cholesterol to HDL cholesterol.

Although saturated fats increase LDL-C, they reduce the LDL particle number. Total LDL particle number quantifies the concentration of LDL particles in various lipid subfractions and is considered a stronger indicator of CV risk than traditional lipoprotein measures.

As for stearic acid, the allegedly non-cholesterol-raising fat, while it appears to lower LDL-C relative to other SFAs, one analysis concluded that it raised LDL-C, lowered HDL-C, and increased the ratio of total to HDL cholesterol in comparison with unsaturated fatty acids. And this is one of the confounders of much nutrition research—observations about a given nutrient are highly dependent on what you compare it to.’

Which is a long-winded way of saying that everything we have been told about saturated fat, its impact on LDL, and its impact on CVD is – frankly – complete bollocks. And if it is complete bollocks, the Keys equation – which has driven all research in this area for 70 years – is also bollocks.

In truth, all possible combinations of LDL going up, down, and staying the same have been found in dietary studies. But I would like to focus on the most recent study. It formed the basis of an episode of a programme called ‘Trust me I’m a doctor’, on the BBC. Researchers studied the impact of different types of saturated fat on LDL and HDL levels.

‘For the experiment, the team recruited nearly one hundred volunteers, all aged over fifty. They were split into three groups and every day for four weeks each ate fifty grams of coconut oil (about two tablespoons), or fifty grams of olive oil – an unsaturated fat already known to lower bad LDL cholesterol – of fifty grams of butter.

This amount of coconut oil contains more than forty grams of saturated fat, twice the maximum recommended daily amount for women, according to Public Health England, but is the level previous research has revealed is necessary to show measurable changes in blood cholesterol over a four-week period.

Before the experiment, all the volunteers had their bad LDL and good HDL cholesterol measured, as well as their height, waist, blood pressure, weight and body fat percentage. Four weeks later, these tests were repeated.

The group who ate butter saw their bad LDL levels rise by about ten per cent, as expected. But the olive oil and coconut oil saw no rise in bad LDL – despite coconut oil having more saturated fat than butter.’

Even more surprisingly, while butter and olive oil both raised good HDL cholesterol by five per cent, coconut oil raised it by a staggering fifteen per cent, meaning that it seemed to have a more positive effect on cholesterol-related health than olive oil.’

It is worth pointing out that this was the largest study of the kind ever to have been done. This may surprise you, but in many nutritional studies, the number of subjects is often in single digits. In case you are thinking we can simply ignore a study done by the BBC, it was carried out to high standards. It has also since been published in the BMJ.

Equally, I can see no reason why the BBC would have any desire to bias the conclusions in any direction.

What they found was that coconut oil, containing the highest percentage of saturated fat, had absolutely no impact on LDL. But it did raise HDL (so-called ‘good’ cholesterol) by 15%. Which is no surprise. If VLDL goes down, HDL goes up. And in this experiment, they kept everything else the same, but just added saturated fat. A single variable.

Anyway, the thing that interests me most, and the reason for writing this particular blog is that I have come to the realisation that the best way to find the answer to a scientific question is to immerse yourself in the science. I would like to believe the published research because it would be lovely if you could look at a study and believe it to be correct/true/unbiased.

But that is no longer possible, most especially in the connected fields of heart disease, and nutrition.

Dr Richard Horton

It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgement of trusted physicians or authoritative medical guidelines.” Marcia Angell – long-time editor of the NEJM.

‘The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue…science has taken a turn towards darkness.’ Richard Horton – editor of The Lancet.

‘The poor quality of medical research is widely acknowledged, yet disturbingly the leaders of the medical profession seem only minimally concerned about the problems and make no apparent efforts to find a solution.’ Richard Smith – long time editor of the BMJ.

It is always, of course, risky to base your thinking and conclusions on what is known about the basic science. New facts can come along to upend your thinking at any time. However, with mainstream medical research in such a corrupt mess, I do not know how else to do it.

The basic research tells us that there is no mechanism whereby saturated fat can raise LDL levels. And the research, such as it can be disentangled, appears to fully support this.

I looked at this blog again, and again, and I thought: Why did I write it…for sure? I wrote it because I wanted to make you aware of three things.

First, how powerful a thought can be. Saturated fat raises the LDL level, and how difficult this is to shift. The power of a simple idea.

Secondly, so that you can see that the truth is out there. It is not to be found amongst the experts in the field. It cannot be found by reading the research, or the guidelines. But it is out there if you look hard enough.

Third, the mainstream just will not change its mind. A recent conference in Switzerland, organised by the BMJ, and others, tried to discuss the dietary guidelines and the role of saturated fat. I was invited but did not go, as I was working.

Dr Zoë Harcombe went and wrote a blog about it (behind a paywall). As she wrote about the conclusion of the conference:

Fiona (Fiona Godlee, editor of the BMJ) started with: “The point about saturated fat is: the evidence is now looking pretty good, but the guidance hasn’t shifted… there doesn’t seem to have been an enormous ‘mea culpa’ from the scientific community that we got it so wrong. That does surprise me.”

Salim replied: “We got brainwashed by a very questionable study, called The Seven Countries Study, many years ago and it was ingrained in our DNA and generations of us were brought up with that… Somebody said that you need to wait for guidelines committees to die before you can change the guidelines committees”!

Fiona then said: “Maybe one outcome of this meeting would be for this meeting to say ‘that’s gone now’, the science has changed. Am I right Salim? Am I right Dariush? It seems to be that should be an outcome of some sort from this meeting.”

Alas, the UK guidelines committee shows no signs of such change, let alone the ‘mea culpa’ that Fiona suggests might be in order.’

You have to wonder what it will take to create real change here. In spite of the adjustment to US dietary guidelines making it clear that eating cholesterol has little if anything to do with eating cholesterol-rich food, my supermarket still has a thriving low-cholesterol section of spreads and other highly processed concoctions. My doctor still recommends statins because of my high LDL. Even my life insurance is negatively impacted by that.
What needs to happen? How can the old guard admit they were wrong without getting too much cholesterol rich egg-yolk on their faces?

Trouble is that “low fat” is highly profitable because it provides a health halo to cheap ingredients which can then be marked up, and though statins are now largely off patent they remain profitable. Then there are PCSK9s. This one will run and run.

“there doesn’t seem to have been an enormous ‘mea culpa’ from the scientific community that we got it so wrong. “ This is a shame for the science in itself , not to correct one when you know .
But thanks for Men and Women who still have a desire for truth in science such as Kendrick, Malhotra, Lustig , Yourself ,Tim Noakes, Harcombe, Teicholz and many other we as public have this information and make informed decisions .

“In conclusion, we found that the increase in LDL-C resulting from very high saturated fat intake in individuals with a preponderance of small LDL was associated with an increase in apoB, and total, medium-sized, and small LDL particles. These results, in conjunction with previous studies, suggest that saturated fat may have heterogeneous effects on levels of atherogenic LDL particles that may depend on the amount of saturated fat consumed, the dietary context, particularly concomitant carbohydrate intake, and/or predisposition to atherogenic dyslipidemia.”

Adding saturated fat to a high carb diet may not be a good plan. But then neither is adding more carbs.

In the context of low carb intake fat metabolism works quite differently. IMO any effects of dietary fat on lipoproteins is due to the uptake and utilisation of the particles and their contents, not on their creation.

tl:dr when you eat so many carbs that your body is only metabolising glucose the fat is stored for later. When you eat more carbs and later never comes, you never switch to properly metabolising fat, whether dietary or (stored) body fat.

It’s incredible to me that in a serious paper about cholesterol, they stil talk about “good” cholesterol and “bad”cholesteol. When I hear “bad cholesterol” it brings to mind what you’d say to a dog: “Bad cholesterol! Don’t do it again!!”